02 December 2009

Glue atherosclerotic plaques

The culprit of strokes and heart attacks has been foundAlexey Tymoshenko, GZT.ru
British doctors found out that the separation of blood clots capable of clogging blood vessels provokes the TLR2 protein.

The discovery of doctors will allow us to offer ways to combat the dangerous phenomenon, which results in heart attacks and strokes.

Researchers from the Imperial College in London found that the appearance of the TLR2 protein, which is synthesized by lymphocytes (cells of the immune system), in the cells of atherosclerotic plaques leads to inflammation of the vascular wall. At the same time, the probability of plaque detachment increases dramatically. This discovery, according to its authors, will help in the creation of drugs that block the activity of TLR2 and prevent life-threatening inflammation of the patient.

Blockage of blood vessels

Atherosclerotic plaques forming on the walls of blood vessels are dangerous. If they come off, foreign particles that have appeared in the blood can clog another vessel. So, if the vessels of the brain are blocked, a stroke occurs or a heart attack develops if the arteries feeding the heart muscle suffer.

The tissue left without blood supply is deprived of oxygen supply and dies. Sometimes with fatal consequences for the body – in cases when it comes to the vital centers of the brain. Heart attack and stroke are the most common causes of death in developed countries (including Russia), ahead of cancer, life-threatening injuries and infectious diseases.

What does immunity have to do with it?

The TLR2 protein is notable for its specificity: it can be detected only in the blood and cells of the immune system, while many other proteins are found, if not in all, then in most cells of the body. This selectivity is explained by the functions of the protein: until recently it was believed that TLR2 helps lymphocytes in detecting bacteria.

However, as shown by the work published in the journal Circulation (Claudia Monaco et al., Toll-Like Receptor-2 Mediates Inflammation and Matrix Degradation in Human Atherosclerosis), the same protein leads to inflammation of the vascular wall. It was already known from previous studies that TLR2 is synthesized in atherosclerotic plaques. When scientists tried to suppress its activity in experiments with cell culture, the cell culture began to produce significantly fewer inflammatory substances.

And inflammation is not only a process that leads to the separation of the formed plaque. Inflammation is also a natural (sometimes, however, resulting from an error) reaction of the body to the invasion of foreign objects. In this regard, the choice of TLR2 protein by scientists is clear: the researchers did not blindly sort through all the proteins, of which there are more than 10 thousand, but worked within the framework of the theory linking atherosclerosis – a disease of the cardiovascular system with inflammation - an immune response.

Atherosclerosis as inflammation

If it is too early to talk about the practical application of the discovery of British doctors (it is still necessary to learn how to block TLR2 in the cells of atherosclerotic plaques, without affecting the normal functioning of the immune system, if possible), then the view of atherosclerosis as a disease associated with inflammation has already borne some fruit.

Markers of inflammation – substances released into the blood in the presence of an inflammatory reaction in the body – have shown themselves, among other things, as a diagnostic sign of atherosclerosis. Moreover, this relationship also manifests itself at the initial stages of the development of the disease, which makes it possible to detect it more accurately and in a timely manner, focusing not only on the cholesterol content in the blood as a risk factor contributing to the growth of atherosclerotic plaques, but also on the actual signs of vascular damage.

Portal "Eternal youth" http://vechnayamolodost.ru02.12.2009

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